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Microbiology > VIII - Gram-Positive Bacteria > Flashcards

VIII - Gram-Positive Bacteria Flashcards

1
Q

Gram (+) cocci in grape-like clusters, β-hemolytic yellow or golden colonies on blood agar, catalase (+), coagulase (+)

A

Staphylococcus aureus

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2
Q

Staphylococcus aureus is cultured in _____ because of salt tolerance.

A

Mannitol Salt Agar

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3
Q

The gold color of Staphylococcus aureus is due to

A

staphyloxanthin

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4
Q

S. aureus: Location

A

human nose (anterior nares), skin

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5
Q

S. aureus: Transmission

A

direct contact (hands), fomites, contaminated food

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6
Q

S. aureus Immunomodulators: Prevents complement activation

A

Protein A

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7
Q

S. aureus Immunomodulators: Builds an insoluble fibrin capsule

A

Coagulase

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8
Q

S. aureus Immunomodulators: Toxic to hematopoietic cells

A

Hemolysins (Cytotoxins)

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9
Q

S. aureus Immunomodulators: Specific for White Blood Cells

A

PV Leukocidin

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10
Q

S. aureus Immunomodulators: Detoxifies hydrogen peroxide

A

Catalase

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11
Q

S. aureus Immunomodulators: Inactivates penicillin derivatives

A

Penicillinase

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12
Q

S. aureus Tissue Penetrance: Hydrolyzes hyaluronic acid

A

Hyaluronidase

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13
Q

S. aureus Tissue Penetrance: Dissolves fibrin clots

A

Fibrinolysin (Staphylokinase)

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14
Q

S. aureus Tissue Penetrance: Spread in fat-containing areas of the body

A

Lipase

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15
Q

S. aureus Toxins: Causes epidermal separation

A

Exfoliatin

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16
Q

S. aureus Toxins: Superantigens causing food poisoning

A

Enterotoxins (heat-stable)

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17
Q

S. aureus Toxins: Superantigen leading to toxic shock syndrome

A

Toxic Shock Syndrome Toxin (TSST-1)

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18
Q

S. aureus Toxins: Causes marked necrosis of the skin and hemolysis

A

Alpha Toxin

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19
Q

S. aureus Pyogenic Disease: Skin and Soft Tissue

A

bullous impetigo, folliculitis, furuncles, carbuncles, cellulitis, hidradenitis suppurativa, mastitis, surgical site infections

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20
Q

Bullous impetigo, foliculitis, furuncles, carbuncles, cellulitis, hidradenitis suppurativa, mastitis, surgical site infections

A

Staphylococcus aureus

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21
Q

Most common cause of acute endocarditis

A

Staphylococcus aureus

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22
Q

Acute endocarditis usually affects _____ in _____.

A

native tricuspid valve, IV drug users

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23
Q

S. aureus Pyogenic Disease: Pneumonia

A

nosocomial pneumonia, VAP, necrotizing pneumonia, complicated by empyema, abscess or pneumatocoele, post-viral

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24
Q

Nosocomial pneumonia, VAP, necrotizing pneumonia, complicated by empyema, abscess or pneumatocoele, post-viral

A

Staphylococcus aureus

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25
Q

Osteomyelitis and septic arthritis come from _____ spread or _____ at the wound site.

A

hematogenous spread, local introduction

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26
Q

Sequestered focus of osteomyelitis arising in the metaphyseal area of a long bone

A

Brodie Abscess

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27
Q

S. aureus: Pyogenic Infections

A

skin, soft tissue, acute endocarditis, pneumonia, osteomyelitis, septic arthritis

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28
Q

S. aureus: Toxigenic Infections

A

gastroenteritis, Scalded Skin Syndrome (Ritter Disease), Toxic Shock Syndrome

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29
Q

Gastroenteritis has _____ onset of vomiting and diarrhea due to ingestion of _____ from _____.

A

acute (4 hours), preformed heat-stable enterotoxin from S. aureus, salad with mayonnaise

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30
Q

S. aureus exfoliatin cleaves _____ in desmosomes leading to separation of epidermis in the _____ causing _____.

A

desmoglein, stratum granulosum, Scalded Skin Syndrome (Ritter disease)

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31
Q

Separation of the dermo-epidermal junction

A

Toxic Epidermal Necrolysis (Lyell Disease)

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32
Q

Fever, hypotension, sloughing of the filiform papillae → strawberry tongue, desquamating rash, multiorgan involvement (>3), usually no site of pyogenic inflammation, blood CS (-)

A

Toxic Shock Syndrome (S. aureus)

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33
Q

Seen in tampon-using menstruating women or in patients with nasal packing for epistaxis

A

Toxic Shock Syndrome (S. aureus)

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34
Q

Methicillin-Sensitive SA (MSSA): Treatment

A

penicillinase-resistant penicillins (nafcillin, oxacillin, dicloxacillin)

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35
Q

Methicillin-Resistant SA (MRSA): Treatment

A

Vancomycin

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36
Q

Vancomycin-Resistant SA (MRSA): Treatment

A

Linezolid

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37
Q

Staphylococcus aureus with altered penicillin binding proteins

A

Methicillin-Resistant SA (MRSA

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38
Q

Gram (+) cocci in clusters, catalase (+), coagulase (-), novobiocin-sensitive, whitish, non-hemolytic colonies on blood agar

A

Staphylococcus epidermidis

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39
Q

S. epidermidis: Location

A

normal skin flora

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40
Q

S. epidermidis: Transmission

A

autoinfection, direct contact (hands)

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41
Q

S. epidermidis is a ___-virulence organism with _____ which adheres well to foreign bodies and form biofilms.

A

low-virulence, glycocalyx

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42
Q

Most common cause of prosthetic valve endocarditis

A

Staphylococcus epidermidis

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43
Q

Most common cause of septic arthritis in prosthetic joints

A

Staphylococcus epidermidis

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44
Q

Most common cause of ventriculoperitoneal shunt infections

A

Staphylococcus epidermidis

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45
Q

S. epidermidis: Treatment

A

removal of prosthetic device, Vancomycin (over 50% are methicillin-resistant)

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46
Q

Gram (+) cocci in clusters, catalase (+), coagulase (-), novobiocin-resistant, whitish, non-hemolytic colonies on blood agar

A

Staphylococcus saprophyticus

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47
Q

2nd most common cause of UTI in sexually active women

A

Staphylococcus saprophyticus

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48
Q

S. saprophyticus: Findings

A

dysuria, pyuria, bacteriuria

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49
Q

S. saprophyticus: Treatment

A

TMP-SMX, quinolones

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50
Q

Gram (+) cocci in chains, β-hemolytic, catalase (-), bacitracin-sensitive, Lancefield group A, PYR test (rapid identification)

A

Streptococcus pyogenes (GABHS)

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51
Q

S. pyogenes: Location

A

human throat (oropharynx), skin

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52
Q

S. pyogenes: Transmission

A

respiratory droplets

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53
Q

S. pyogenes Virulence Enzymes: Degrades hyaluronic acid (spreading factor)

A

Hyaluronidase

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54
Q

S. pyogenes Virulence Enzymes: Activates plasminogen

A

Streptokinase (Fibrinolysin)

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55
Q

S. pyogenes Virulence Enzymes: Degrades DNA in exudates or necrotic tissue

A

DNAse (Streptodornase)

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56
Q

S. pyogenes Virulence Enzymes: Inactivates complement C5A

A

C5A Peptidase

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57
Q

S. pyogenes Toxins: Produces scarlet fever

A

Erythrogenic Toxin

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58
Q

S. pyogenes Toxins: Highly antigenic, causes AB formation

A

Streptolysin O (oxygen-labile)

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59
Q

S. pyogenes Toxins: Oxygen-stable

A

Streptolysin S

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60
Q

S. pyogenes Toxins: Superantigen similar to TSST

A

Pyogenic Exotoxin A

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61
Q

S. pyogenes Toxins: Protease that rapidly destroys tissue → necrotizing fascitis

A

Exotoxin B

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62
Q

Document antecedent S. pyogenes pharyngitis

A

Anti-Streptolysin O (ASO)

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63
Q

Document antecedent S. pyogenes skin infection

A

Anti-DNAse B

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64
Q

Streptolysin O is irreversibly inhibited by

A

cholesterol in skin lipids

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65
Q

Decrease the efficacy of streptokinase in managing MI

A

Anti-Streptokinase Antibodies

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66
Q

S. pyogenes: Pyogenic Infections

A

impetigo contagiosa, erysipelas, cellulitis, necrotizing fascitis, pharyngitis

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67
Q

Impetigo contagiosa, erysipelas, cellulitis, necrotizing fascitis, pharyngitis

A

Streptococcus pyogenes

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68
Q

Perioral blistered lesions with honey-colored crust, accumulation of neutrophils beneath stratum corneum, PSGN

A

Impetigo Contagiosa

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69
Q

Superficial infection extending into dermal lymphatics

A

Erysipelas

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70
Q

Deeper infection involving subcutaneous/dermal tissues, facilitated by hyaluronidase (spreading factor)

A

Cellulitis

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71
Q

Rapidly progressive infection of deep subcutaneous tissues, facilitated by exotoxin B

A

Necrotizing Fascitis

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72
Q

Most common bacterial cause of sore throat

A

Streptococcus pyogenes

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73
Q

Pharyngeal inflammation, exudate, fever, leukocytosis, tender CLAD

A

Pharyngitis

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74
Q

Pyogenic Complications of Pharyngitis

A

abscess, otitis, sinusitis, meningitis

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75
Q

Post-pharyngitic, due to erythrogenic toxin, seen in lysogenized strains, fever, strawberry tongue, centrifugal rash (sandpaper-like), Pastia’s lines, desquamation

A

Scarlet Fever

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76
Q

Test for Scarlet Fever Susceptibility

A

Dick Test

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77
Q

Clinically similar but milder than S. aureus TSS, due to pyogenic exotoxin A, recognizable site of pyogenic inflammation, blood culture (+)

A

Streptococcal Toxic Shock Syndrome

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78
Q

S. pyogenes: Toxigenic Infections

A

scarlet fever, strep. TSS

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79
Q

S. pyogenes: Immunologic Infections

A

ARF, GN

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80
Q

Post-pharyngitic, cross-reacting antibodies to M proteins and antigens of the joints, heart and brain

A

Acute Rheumatic Fever

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81
Q

Jones Criteria

A

migratory polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, Sydenham chorea

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82
Q

Post-pharyngitic or post-impetigo, M protein incites immune complex deposition on the glomerular basement membrane

A

Post-Strep Glomerulonephritis

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83
Q

Post-Strep Glomerulonephritis: Findings

A

hypertension, periorbital edema, hematuria

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84
Q

Post-Strep Glomerulonephritis: Treatment

A

IV Pen G, antibiotic prophylaxis for patients with hx of RF

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85
Q

Gram (+) cocci in chains, β-hemolytic, catalase (-), bacitracin-resistant, hydrolyze hippurate, CAMP test (+), Lancefield group B, LIM broth

A

Streptococcus agalactiae (GBS)

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86
Q

S. agalactiae: Location

A

vagina

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87
Q

S. agalactiae: Transmission

A

transvaginal, transplacental

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88
Q

S. agalactiae: Pyogenic Infections

A

UTI in pregnant women, neonatal pneumonia, neonatal sepsis, neonatal meningitis, endometritis (polymicrobial, foul-smelling lochia)

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89
Q

Most common cause of neonatal pneumonia, sepsis and meningitis worldwide

A

Streptococcus agalactiae (GBS)

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90
Q

Most common cause of neonatal pneumonia, sepsis and meningitis in the Philippines

A

Escherichia coli

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91
Q

Predisposing Factors for Neonatal GBS Infection

A

intrapartum fever (>38°C), PROM (>18h), vaginal colonization, complement deficiency

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92
Q

S. agalactiae: Treatment

A

Penicillin G (+ aminoglycoside for serious infections)

93
Q

All pregnant women should be screened for GBS colonization at

A

35-37 weeks AOG

94
Q

S. agalactiae: Treatment for Pregnant Women

A

chemoprophylaxis with IV Penicillin or Ampicillin 4 hours prior to delivery

95
Q

Gram (+) cocci in chains, catalase (-), γ-hemolytic (non-hemolytic) colonies, Lancefield group D, bile and optochin-resistant, hydrolyzes esculin in bile-esculin agar (BEA), PYR test (+)

A

Group D Streptococci (Enterococcus faecalis)

96
Q

E. faecalis can grow in

A

6.5% NaCl

97
Q

Enterococcus which cannot grow in 6.5% NaCl

A

S. bovis

98
Q

Group D Streptococci: Location

A

colon, urethra, female GUT, may enter bloodstream during GUT/GIT procedures

99
Q

Group D Streptococci: Diseases

A

UTIs due to indwelling catheters and GUT instrumentation, biliary tract infections, endocarditis in patients who underwent GIT surgery, marantic endocarditis in patients with abdominal malignancy (colorectal/pancreatic)

100
Q

Cause of Marantic Endocarditis

A

Streptococcus bovis

101
Q

Group D Streptococci: Treatment

A

Penicillin + Gentamicin, Vancomycin (penicillin resistance), Linezolid (vancomycin resistance)

102
Q

Gram (+) lancet-shaped cocci in pairs or short chains, catalase (-), α-hemolytic, bile and optochin-sensitive, prominent polysaccharide capsule, (+) Quellung reaction

A

Streptococcus pneumoniae

103
Q

Encapsulated Bacteria

A

Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa, Neisseria meningitidis, Salmonella typhi, B group Streptococci

104
Q

S. pneumoniae: Location

A

upper respiratory tract

105
Q

S. pneumoniae: Transmission

A

respiratory droplets

106
Q

S. pneumoniae: Pathogenesis

A

capsule - retards phagocytosis, IgA protease - colonization, c-substance - reacts with CRP

107
Q

S. pneumoniae: Pyogenic Infections

A

pneumonia, otitis media, sinusitis, bacterial meningitis, septic shock

108
Q

Most common cause of CAP

A

Streptococcus pneumoniae

109
Q

Sudden chills, fever, productive cough (rust-colored sputum), pleuritic chest pain, lobar pattern

A

Pneumonia (S. pneumoniae)

110
Q

Most common cause of otitis media, sinusitis and bacterial meningitis

A

Streptococcus pneumoniae

111
Q

Skull fracture with spinal fluid leakage from the nose predisposes to

A

Meningitis (S. pneumoniae)

112
Q

Splenectomy predisposes to _____ shock.

A

septic shock

113
Q

S. pneumoniae: Treatment

A

Penicillin G, Amoxicillin (Philippines), Levofloxacin or Vancomycin + Ceftriaxone (penicillin resistance)

114
Q

S. pneumoniae: Prevention

A

polyvalent (23-type) polysaccharide vaccine - capsule, conjugated vaccine - pneumococcal polysaccharide coupled with carrier protein (diptheria toxoid - enhances immunogenicity)

115
Q

Gram (+) cocci in chains, catalase (-), α-hemolytic, bile and optochin-resistant

A

Viridans Streptococci (S. mutans, S. sanguis)

116
Q

Viridans Streptococci: Location

A

oropharynx (normal flora), enters bloodstream during dental procedure (Amoxicillin/Erythromycin prophylaxis)

117
Q

Viridans Streptococci have _____ which enhances adhesion to damage heart valves

A

glycocalyx

118
Q

Viridans Streptococci are protected from host defenses within

A

vegetations

119
Q

Viridans Streptococci: Dental caries, plaque

A

S. mutans

120
Q

Viridans Streptococci: Subacute endocarditis (SBE)

A

S. sanguis

121
Q

Viridans Streptococci: Brain abscess

A

S. intermedius

122
Q

Most common cause for subacute endocarditis and native valve endocarditis

A

S. sanguis (Viridans Streptococci)

123
Q

Viridans Streptococci: Treatment

A

Penicillin G ± aminoglycoside (Gentamicin), Vancomycin (penicillin resistance), Linezolid (vancomycin resistance)

124
Q

Spore-forming gram (+) rods, aerobic, non-motile, box-car-shaped, Medusa head morphology (dry ground glass surface and irregular edges with projections along lines of inoculation)

A

Bacillus anthracis

125
Q

Bacillus anthracis: Location

A

soil

126
Q

Bacillus anthracis: Transmission

A

contact with infected animals, inhalation of spores from animal hair and wool (woolsorter’s disease)

127
Q

Woolsorter’s Disease

A

Bacillus anthracis

128
Q

Bacillus anthracis Virulence Factors: Antiphagocytic capsule

A

Poly-D-Glutamate

129
Q

Bacillus anthracis Virulence Factors: Calmodulin-dependent adenylate cyclase

A

Edema Factor (EF) - A subunit, cellular swelling

130
Q

Bacillus anthracis Virulence Factors: Inhibits a signal transduction in cell division

A

Lethal Factor (LF) - A subunit

131
Q

Bacillus anthracis Virulence Factors: Mediates the entry of EF and LF into the cell

A

Protective Antigen (PA) - B subunit

132
Q

Protective Antigen + Edema Factor =

A

Edema Toxin

133
Q

Protective Antigen + Lethal Factor =

A

Lethal Toxin

134
Q

Bacillus anthracis: Diseases

A

cutaneous, inhalational, GI

135
Q

Direct epidermal contact with spores causes formation of a malignant pustules with subsequent eschar and central necrosis, 20% mortality

A

Cutaneous Anthrax

136
Q

Inhaled spores from animals (woolsorter’s disease) or from weaponized preparations (bioterrorism), prolonged latent period (2 mos.) before rapid deterioration, massively enlarged mediastinal LN, pulmonary hemorrhage, meningeal symptoms, 100% mortality rate without immediate treatment

A

Inhalational Anthrax

137
Q

Ingestion of live spores leads to UGI ulceration, edema and sepsis (rapidly prorgressive), mortality rate approaches 100%

A

GI Anthrax

138
Q

Cutaneous Anthrax: Treatment

A

Ciprofloxacin

139
Q

Inhalational/GI Anthrax: Treatment

A

Ciprofloxacin or Doxycycline + 1 or 2 additional antibiotics (rifampin, vancomycin, penicillin, imipenem, clindamycin, clarithromycin)

140
Q

Spore-forming gram (+) rods, aerobic, motile, reheated fried rice

A

Bacillus cereus

141
Q

Bacillus cereus: Location

A

spores on grains such as rice survive steaming and rapid frying, spores germinate when rice is kept warm for many hours

142
Q

Chinese Fried Rice Syndrome

A

Bacillus cereus

143
Q

Cholera-like enterotoxin that causes ADP-ribosylation increasing cAMP, secretory diarrhea, long incubation period

A

Heat-Labile Enterotoxin (Bacillus cereus)

144
Q

Staphylococcal-like enterotoxin which functions as a superantigen, food poisoning, emetic, short incubation period

A

Heat-Stable Enterotoxin (Bacillus cereus)

145
Q

Bacillus cereus: Diseases

A

emetic form, diarrheal form, ophthalmitis

146
Q

Short incubation period (4 hours), consists primarily of nausea and vomiting, similar to staphylococcal food poisoning

A

Emetic Form of Bacillus cereus

147
Q

Long incubation period (18 hours), watery, non-bloody diarrhea, resembling clostridial gastroenteritis

A

Diarrheal Form of Bacillus cereus

148
Q

Occurs after traumatic penetrating eye injuries with a soil-contaminated object, complete loss of light perception within 48 hours of the injury

A

Bacillus cereus Ophthalmitis

149
Q

Bacillus cereus: Rice

A

Emetic Form

150
Q

Bacillus cereus: < 6 hours incubation period (mean = 2h)

A

Emetic Form

151
Q

Bacillus cereus: Vomiting, nausea, abdominal cramps

A

Emetic Form

152
Q

Bacillus cereus: 8-10 hours duration (mean = 9h)

A

Emetic Form

153
Q

Bacillus cereus: Uses heat-stable enterotoxin

A

Emetic Form

154
Q

Bacillus cereus: Meat, vegetables

A

Diarrheal Form

155
Q

Bacillus cereus: > 6 hours incubation period (mean = 9h)

A

Diarrheal Form

156
Q

Bacillus cereus: Diarrhea, nausea, abdominal cramps

A

Diarrheal Form

157
Q

Bacillus cereus: 20-36 hours duration (mean = 24h)

A

Diarrheal Form

158
Q

Bacillus cereus: Uses heat-labile enterotoxin

A

Diarrheal Form

159
Q

Food Poisoning: Treatment

A

symptomatic

160
Q

B. cereus Ophthalmitis: Treatment

A

Vancomycin (emergency, -cidal), Clindamycin (-cidal at high doses), Ciprofloxacin, Gentamicin

161
Q

Spore-forming gram (+) rods, anaerobic, tennis-racket-like (spore is at one end - terminal spore)

A

Clostridium tetani

162
Q

Clostridium tetani: Location

A

soil

163
Q

Clostridium tetani: Transmission

A

traumatic breaks in skin - skin popping in IV drug abuse, stepping on a nail

164
Q

Protease that cleaves proteins involved in the release of glycine from Renshaw cells in the spinal cord

A

Tetanus Toxin (tetanospasmin)

165
Q

Clostridium tetani: Findings

A

strong muscle spasms (spastic paralysis, tetany), lockjaw (trismus), risus sardonicus (smile of death), opisthotonos (extension of vertebral muscles), respiratory failure

166
Q

Clostridium tetani: Treatment

A

debridement of primary wound, Penicillin G

167
Q

Clostridium tetani: Prevention

A

ATS - passive immunization, Tetanus Toxoid - vaccination (every 10 years)

168
Q

Spore-forming gram (+) rods, anaerobic, bulging cans

A

Clostridium botulinum

169
Q

Clostridium botulinum: Location

A

soil

170
Q

Clostridium botulinum: Transmission

A

improperly preserved food, alkaline vegetables (green beans, peppers, mushrooms), smoked fish, canned goods (bulging), honey (raw)

171
Q

Heat-labile toxin that blocks acetylcholine release causing flaccid paralysis (descending pattern)

A

Botulinum Toxin

172
Q

Most common immunologic types of botulinum toxin in humans (out of 8)

A

A, B, E

173
Q

Commercial preparation of botulinum toxin (exotoxin A)

A

Botox - wrinkle removal, torticollis, achalasia, hyperhydrosis

174
Q

Clostridium botulinum: Toxigenic Infections

A

food-borne, infant (Floppy Baby Syndrome), wound

175
Q

Food-Borne Botulism: Findings

A

eye symptoms, bulbar signs, anticholinergic effects, bilateral descending flaccid paralysis, respiratory paralysis

176
Q

BOV, diplopia, ptosis, mydriasis, dysphonia, dysarthria, dysphagia, dry mouth, constipation, abdominal pain, bilateral descending flaccid paralysis, respiratory paralysis

A

Food-Borne Botulism

177
Q

Food-Borne Botulism: Eye Symptoms

A

BOV, diplopia, ptosis, mydriasis

178
Q

Food-Borne Botulism: Bulbar Signs

A

diplopia, dysphonia, dysarthria, dysphagia

179
Q

Food-Borne Botulism: Anticholinergic Effects

A

dry mouth, constipation, abdominal pain

180
Q

Triad of Botulism

A

symmetric descending flaccid paralysis (prominent bulbar involvement), absence of fever, intact sensorium

181
Q

When babies ingest spores found in household dust or honey, due to the absence of competitive bowel microbes

A

Infant Botulism (Floppy Baby Syndrome)

182
Q

Traumatic implantation and germination of Clostridium botulinum spores at the wound site

A

Wound Botulism

183
Q

Clostridium botulinum: Treatment

A

elimination of the organism from the GIT (gastric lavage, metronidazole or penicillin), ventilatory support, trivalent botulinum antitoxin (A, B, E)

184
Q

Clostridium botulinum: Prevention

A

proper sterilization of all canned and vacuum-packed foods, adequate cooking, discard bulging/swollen cans

185
Q

Spore-forming gram (+) rods, anaerobic, gas-forming, double-hemolysis on blood agar, growth on egg yolk (lecithinase), non-motile but with rapidly spreading growth on culture media

A

Clostridium perfringens

186
Q

Clostridium perfringens: Location

A

soil, colon

187
Q

Clostridium perfringens: Transmission

A

contamination of wound with soil or feces (myonecrosis), ingestion of contaminated food (food poisoning)

188
Q

A lecithinase that cleaves cell membranes

A

Alpha Toxin

189
Q

Pain, edema, cellulitis with crepitation from gas produced by anaerobic metabolism, hemolysis, jaundice

A

Gas Gangrene (Clostridium perfringens)

190
Q

Production of enterotoxin which acts as superantigen, 8-16 hour incubation period, watery diarrhea with cramps and little vomiting resolves within 24 hours

A

Clostridium perfringens Food Poisoning

191
Q

Clostridium perfringens: Treatment

A

gas gangrene - wound debridement, Penicillin, food poisoning - supportive

192
Q

Clostridium perfringens: Prevention

A

proper wound care, adequate cooking

193
Q

Spore-forming gram (+) rods, anaerobic, psudomembranes, exotoxin in stool detected by cytopathic effect on cultured cells or ELISA, exotoxin A & B

A

Clostridium difficile

194
Q

Clostridium difficile: Location

A

colon - 3% of population, 30% of hospitalized patients

195
Q

Clostridium difficile: Transmission

A

fecal-oral route, hands of hospital personnel

196
Q

Antibiotics suppress normal GI flora allowing _____ to grow.

A

Clostridium difficile

197
Q

Antibiotics that suppress normal GI flora allowing Clostridium difficile to grow.

A

clindamycin, cephalosporins (2nd & 3rd gen.), ampicillin

198
Q

Inhibit GTPases leading to apoptosis and death of enterocytes, results in pseudomembranes

A

Exotoxins A & B

199
Q

Clostridium difficile can precipitate flare-ups of

A

ulcerative colitis

200
Q

Non-bloody diarrhea associated with pseudomembranes (yellow-white plaques) on the colonic mucosa, toxic megacolon can occur

A

Pseudomembranous Colitis

201
Q

Cause of Pseudomembranous Colitis

A

Clostridium difficile

202
Q

Cause of Pseudomembranous Pharyngitis

A

Diphtheria

203
Q

Cause of Pseudomembranous Esophagitis

A

Candida

204
Q

Clostridium difficile: Treatment

A

causative antibiotic should be withdrawn, oral metronidazole or vancomycin, fluid replacement, surgery - toxic megacolon

205
Q

Non-spore-forming gram (+) rods, aerobic, non-motile, curved, Chinese characters, club or comma-shaped arranged in V or L formations, metachromatic granules (Babes-Ernst/volutin), black colonies on tellurite plate, toxigenicity detected using modified Elek’s test

A

Corynebacterium diphtheriae

206
Q

Corynebacterium diphtheriae: Location

A

throat

207
Q

Corynebacterium diphtheriae: Transmission

A

respiratory droplets

208
Q

Corynebacterium diphtheriae exotoxin inhibits protein synthesis by adding ADP-ribose to

A

elongation factor-2 (EF-2)

209
Q

Elongation Factor-2: Has ADP-ribosylating activity

A

A subunit

210
Q

Elongation Factor-2: Binds the toxin to cell surface

A

B subunit

211
Q

Elongation Factor-2 is encoded by

A

β-prophage

212
Q

Result from the death of mucosal epithelial cells

A

pseudomembrane

213
Q

Diphtheria (ABCDEFG)

A

ADP-ribosylation, Beta-prophage, Corynebacterium, Diphtheriae, Elongation Factor-2, Granules (metachromatic)

214
Q

Beta-Prophage Encoded Toxins

A

Shiga-like toxin (EHEC), Botulinum toxin, Cholera toxin, Diphtheria toxin, Erythrogenic toxin (S. Pyogenes)

215
Q

Prominent, thick, gray pseudomembranes over tonsils and throat, airway obstruction, myocarditis, cranial nerve and/or muscle paralysis

A

Corynebacterium diphtheriae

216
Q

Corynebacterium diphtheriae: Treatment

A

antitoxin, Penicillin G

217
Q

Corynebacterium diphtheriae: Prevention

A

toxoid vaccine in combination with tetanus toxoid and pertussis vaccine (DTaP)

218
Q

Non-spore-forming gram (+) rods, aerobic, curved, tumbling motility, arranged in V or L formations, narrow zone of β-hemolysis, paradoxical growth in cold temperature (cold enhancement, 18°C)

A

Listeria monocytogenes

219
Q

Listeria monocytogenes: Location

A

GI, female GUT, animals, plants, soil

220
Q

Listeria monocytogenes: Transmission

A

transplacental, contact during delivery, unpasteurized dairy

221
Q

Interacts with E-cadherin on the surface of cells

A

Internalin

222
Q

Allows escape of Listeria monocytogenes from phagosomes

A

Listeriolysin

223
Q

Propels the bacteria through the membrane of one human cell to another

A

Actin Rockets

224
Q

Transplacental transmission, late miscarriage or birth complicated by sepsis, multiorgan abscesses and disseminated granulomas

A

Early-Onset Neonatal Listeriosis (Granulomatosis Infantiseptica)

225
Q

Listeria transmitted during childbirth, meningitis or meningoencephalitis

A

Late-Onset Neonatal Listeriosis

226
Q

Listeria bacteremia, sepsis, meningitis in the pregnant, elderly, immunocompromised

A

Adult Listeriosis

227
Q

Listeria monocytogenes: Treatment

A

Ampicillin ± Gentamicin

228
Q

Listeria monocytogenes: Prevention

A

pregnant women and immunocompromised patients should not ingest unpasteurized milk products or raw vegetables

Microbiology (17 decks)

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